Year: 2002
Type: article
Abstract: Central administration of glucagon-like peptide-1 (GLP-1) produces responses similar to those produced by a toxic LiCl dose, the prototypical visceral illness-inducing agent.These responses include anorexia, conditioned taste aversion (CTA) learning and distinct Fos activation.Importantly, in the rat, LiCl administration Fos activates a significant number of preproglucagon-producing cells.Additionally, in the rat, pretreatment with a GLP-1 receptor (GLP-1R) antagonist attenuates these illness responses.Together, these data led to the hypothesis that the central GLP-1 system mediates visceral illness.To further describe GLP-1 action in visceral illness, we determined LiCl ability to elicit anorexia, CTA learning and Fos activation in mice lacking GLP-1 signaling (GLP-1R -/-) expecting these responses would be absent or attenuated.Consistent with this prediction, GLP-1R -/-mice exhibit reduced Fos activation in brain regions downstream of GLP-1R signaling compared to +/+ controls.In contrast to our prediction, GLP-1R -/-mice are anorectic and form a CTA in response to LiCl.These data support the idea that there is a species difference between mouse and rat for the Conditioned Taste Aversion Sodium Appetite Pica Oxytocin Secretion CNS Involvement in Visceral Illness LiCl GLP-1 and Visceral Illness Actions of Exendin-4 and Exendin-9 GLP-1R -/-Mice Summary Chapter 1: The Effect of Lithium Chloride in Mice with a Targeted Deletion of the Glucagon-Like Peptide-1 Receptor Chapter 2: LiCl Administration Does Not Fos Activate Wild-Type Preproglucagon-Producing Cells and Glucagon-Like Peptide-1 Supports Conditioned Taste Aversion Learning in Wild-Type Mice but not in Mice with a Targeted Deletion of the Glucagon-Like Peptide-1 Receptor Chapter 3: Mice with a Targeted Deletion of the Glucagon-Like Peptide-1 Receptor Exhibit Cholecystokinin Anorexia and Have Increased Body Adiposity Discussion and Future Directions
Author: Jennifer Lachey
Institution: University of Cincinnati
Language: English
Subfield: Endocrine and Autonomic Systems
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2485492127